Coronary heart disease is generally thought to be caused by the narrowing of coronary arteries by atherosclerosis, the buildup of fatty deposits in the lining of the arteries. The process that may lead to atherosclerosis begins with the accumulation of excess lipids and cholesterol in the blood. These substances infiltrate the lining of arteries, gradually increasing in size to form deposits commonly referred to as plaque or atherosclerotic occlusions. Plaques narrow the arterial lumen and impede blood flow. Thrombus can accumulate on the lesion, eventually creating a blood clot that may block the artery completely.
The phenomenon of “vulnerable plaque” has created new challenges in recent years for the treatment of heart disease. Unlike occlusive plaques that impede blood flow, vulnerable plaque develops within the arterial walls, but it often does so without the characteristic substantial narrowing of the arterial lumen and resulting symptoms. As such, conventional methods for detecting heart disease, such as an angiogram, may not detect vulnerable plaque growth into the arterial wall. After death, histological examination of the heart can reveal the presence of intact and ruptured vulnerable plaques in the coronary arteries.
The intrinsic histological features that may characterize a vulnerable plaque include increased lipid content, increased macrophage, foam cell and T-lymphocyte content, and reduced collagen and smooth muscle cell (“SMC”) content. This fibroatheroma type of vulnerable plaque is often referred to as “soft,” having a large lipid pool covered by a fibrous cap. The fibrous cap contains mostly collagen, whose reduced concentration combined with macrophage derived enzyme degradation can cause the fibrous cap of these lesions to rupture under unpredictable circumstances. When ruptured, the lipid core contents, thought to include tissue factor, contact the arterial bloodstream, cause a blood clot to form that can completely block the artery resulting in an acute coronary syndrome (“ACS”) event. This type of atherosclerosis is coined “vulnerable” because of the unpredictable tendency of the plaque to rupture. It is thought that hemodynamic and cardiac forces, which yield circumferential stress, shear stress, and flexion stress, may cause disruption of a fibroatheroma type of vulnerable plaque. These forces may rise as the result of simple movements, such as getting out of bed in the morning, or in vivo forces related to blood flow and the beating of the heart. It is thought that plaque vulnerability in fibroatheroma types is determined primarily by factors which include: (1) size and consistency of the lipid core; (2) thickness of the fibrous cap covering the lipid core; and (3) inflammation and repair within the fibrous cap.
FIGS. 1A-1C illustrate the bursting of a vulnerable plaque and the blockage of blood flow by the resulting scar tissue. FIG. 1A illustrates the growth of a vulnerable plaque within the vessel wall. As is typical of vulnerable plaque, it does not extend far out into the vessel lumen to obstruct blood flow (as indicated by the directional arrows). FIG. 1B illustrates the rupturing of the vulnerable plaque, and in this case, in a direction against blood flow. This event alone may cause an occlusive thrombosis. Alternatively, the ruptured contents may be washed downstream by the blood flow (if the ruptured contents are relatively small) without any harmful effects. However, as illustrated by FIG. 1C, the fibrous cap that remains as dissected edges, and torn flaps, can protrude into the blood flow, or even form pockets that further increase the chances of an occlusive clot formation. The interior lining of the fibrous cap, and lipid pool, has no coverage of endothelial cells. In addition to mechanical obstructions, all of these surfaces are highly thrombogenic. As such, the therapeutic rupture of a vulnerable plaque might be a viable treatment method if not for the uncontrolled mechanics of the rupture, exposing thrombogenic surfaces, creating issue flaps and dissection, and even forming occlusive pockets. The prior art does not provide for a device or technique to treat vulnerable plaque by rupturing it in a controlled manner while minimizing harmful side effects.